Glicirricina

Glycyrrhizin

1. Identity

1.1 Nomenclature and Chemical Nature

Glycyrrhizinic acid — also widely referred to as glycyrrhizin — is a triterpenoid saponin obtained from the root and rhizome extracts of liquorice (Glycyrrhiza glabra). The World Health Organization (WHO) has recommended that the compound be named "glycyrrhizinic acid," noting that "glycyrrhizin" is more correctly the name given to the licorice extract itself rather than the purified saponin; in practice, however, the two terms are used interchangeably throughout the scientific literature.

Glycyrrhizin is defined as a pentacyclic triterpenoid saponin compound that serves as a bioactive ingredient in licorice, exhibiting pharmacological activities such as anti-inflammatory, antitumor, and hepatoprotection, while also being utilized as a sweetener due to its approximately 170-fold greater sweetness than sucrose. It is an amphiphilic triterpenoid composed of a hydrophobic aglycone conjugated to hydrophilic glucuronic acid residues, enabling interaction with both aqueous environments and lipid membranes.

The main chemical constituents of licorice are triterpene saponins, of which glycyrrhizin is the principal component. Glycyrrhizin is a glycoside occurring as a mixture of calcium, sodium, and potassium salts of glycyrrhizinic acid. Following hydrolysis, it releases two molecules of d-glucuronic acid and the aglycone 18β-glycyrrhetinic acid. This triterpenic aglycone is also known by the pharmaceutical name "enoxolone."

The genus name Glycyrrhiza is derived from the ancient Greek for "sweet root" (glykos meaning sweet; rhiza meaning root), which was later Latinized to liquiritia and eventually to "licorice."

1.2 Botanical Source

Defined as the roots and underground stems of principally three Glycyrrhiza species — G. glabra L., G. uralensis Fish. ex DC., and G. inflata Batalin — licorice has been used as a medicinal herb for millennia and is marketed as root sticks, powders, and other preparations. Glycyrrhiza glabra is a perennial herb native to central and south-western Asia, as well as the Mediterranean region, and is cultivated in temperate and subtropical regions across Europe and Asia.

Glycyrrhizin, a sweet triterpenoid saponin, is found specifically in the roots and stolons of Glycyrrhiza species. Both of the key cytochrome P450 enzymes involved in its biosynthesis (CYP88D6 and CYP72A154) are detected in the roots and stolons, but not in the leaves or stems, which is consistent with the accumulation pattern of glycyrrhizin within the plant. The dried licorice root extract may contain around 4–25% of the saponin, along with other compounds such as polyphenols, saponins, and triterpenes.

1.3 Common Forms and Preparations

The two principal forms in commerce are licorice root (Liquiritiae radix) and the extract (Glycyrrhizae extractum crudum or Succus liquiritiae). In pharmaceutical and clinical contexts, glycyrrhizin is available in several distinct formulations:

• In Japan, Stronger Neo-Minophagen C (SNMC) is a commonly prescribed glycyrrhizin solution administered intravenously for the treatment of chronic hepatitis. SNMC is an intravenous solution comprised of 0.2% glycyrrhizin, 0.1% cysteine, and 2.0% glycine in a saline solution.
• Clinical formulations of glycyrrhizin preparations (GLPs) include diammonium glycyrrhizinate (DG), compound glycyrrhizin (CG), and magnesium isoglycyrrhizinate (MgIG), all represented by their primary active components — 18α- and 18β-glycyrrhetinic acid.
• Further purification using several extraction techniques gives usually the monoammonium glycyrrhizinate salt as the purified product.
• Topical preparations such as dipotassium glycyrrhizate and stearyl glycyrrhetinate are used in cosmetic and dermatological formulations.
• When glycyrrhizin is orally administered it is hydrolyzed by enterobacteria to release its sugar moiety and absorbed as glycyrrhetic acid; to improve its bioavailability, intra-rectal administration in the form of suppositories has been proposed.

Glycyrrhizinic acid is currently considered "Generally Recognized as Safe" (GRAS) by the US Food and Drug Administration, and there are guidelines for maximum permitted levels of the saponin in several preparations.

2. Traditional and Historical Use

2.1 Ancient Cultures

Since the beginning of recorded history, humans have made use of liquorice (mainly Glycyrrhiza glabra L., Leguminosae) as a remedy. Traditions from different geographical regions and different time periods have documented its extensive use. The first documented medicinal use of liquorice can be traced back to ancient Assyrian, Egyptian, Chinese, and Indian cultures. Greek sources provide the first use of liquorice as a drug in Europe.

The earliest documented uses date back to approximately 2500 BCE in Assyrian and Egyptian cultures, where it was employed as an expectorant and digestive remedy. By the time of ancient Greek civilization (4th century BCE) and Chinese medicine (documented around 200 BCE), licorice was prescribed for respiratory ailments, sore throats, and gastrointestinal discomfort.

The ancient Greeks and Romans are known to have cultivated the plants in the third century. Licorice was a prescriptive agent of Hippocrates in the treatment for asthma, dry cough, and other "pectoral diseases," and was also thought to be effective in preventing thirst.

2.2 Traditional Chinese Medicine (TCM)

Glycyrrhiza species are medicinally important leguminous plants, and their thickened main roots and stolons (licorice) have been used extensively in traditional herbal medicine in China for thousands of years. In TCM, licorice root — known as Gancao — was incorporated into multi-herb decoctions to harmonize formulas, moderate the harsh properties of other ingredients, and extend therapeutic effects.

A classical prescription called Shaoyao Gancao decoction, composed of Paeonia lactiflora root and honeyed licorice, was traditionally used to relieve spastic diseases such as gastrointestinal spasm and post-stroke spasm. Sijunzi decoction (SJZD), with licorice as a main herb, was applied for the treatment of spleen deficiency syndrome in TCM, and modern studies have confirmed that SJZD has a significant effect on irritable bowel syndrome, chronic gastritis, and peptic ulcers.

2.3 Other Traditional Systems

Licorice root has a long history of use, going back to ancient Assyrian, Egyptian, Greek, Arab, Chinese, Tibetan, and Indian cultures. It was used in traditional medicine practices for coughing, asthma, and wound healing, as well as for diseases of the lungs, liver, and arteries. In Ayurvedic medicine, the root was used in preparations addressing respiratory and digestive complaints. G. glabra is an old-age medicinal plant belonging to the Leguminosae/Fabaceae family and known as "mulaithi" in north India. The chemical composition of G. glabra has been reported for several pharmacological activities, including expectorant, antidemulcent, antiulcer, anticancer, anti-inflammatory, and antidiabetic uses.

3. Key Constituents and Active Compounds

3.1 Principal Phytochemicals

Active constituents of Glycyrrhiza glabra include saponins (glycyrrhizin, glycyrrhizic acid, α-terpineol), as well as phenolic components such as flavonoids including liquoarylcoumarin, liquiritigenin, and isoliquiritigenin. Other saponins identified in the licorice root include glabasaponins A–G, 30-hydroxyglycyrrhizin, urlasaponins, and 22b-acetoxyl-glycyrrhizin. Many of the biologically active compounds identified are present throughout the entire plant (including the rhizomes) and account in total for 40–50% of the total dry weight.

3.2 Glycyrrhizin and Its Aglycone

From a therapeutic point of view, glycyrrhizin is the main triterpenoid saponin, showing significant anti-inflammatory, antioxidant, immunoregulatory, and antiviral effects. The metabolic processes that take place throughout the plant hydrolyze glycyrrhizin into two pentacyclic triterpenic stereoisomers: 18α- and 18β-glycyrrhetinic acids.

The sugar moiety of glycyrrhizin, which is composed of two glucuronic acids, makes it sweet and is thought to reduce its side effects compared to the aglycone. The saponin has no oral bioavailability as intact glycyrrhizin, being absorbed as glycyrrhetinic acid after hydrolysis of its carbohydrate moiety by intestinal bacteria.

3.3 Mechanisms of Action

Glycyrrhizin preparations exhibit multi-target pharmacological mechanisms comprising anti-inflammatory, membrane-stabilizing, antioxidant, anti-apoptotic, immunomodulatory, and anti-fibrotic effects that collectively underpin their hepatoprotective activity.

Anti-inflammatory actions: Several mechanisms of the glycyrrhizin-induced anti-inflammatory effect are reported, including inhibition of thrombin-induced platelet aggregation, inhibition of prostaglandin E2 production, and inhibition of phospholipase A2 (PLA2). The strongest mechanistic evidence supports antioxidant and anti-inflammatory effects mediated through Nrf2 activation, NF-κB suppression, modulation of Bax/Bcl-2 and caspase signaling, inhibition of CYP2E1-related toxic bioactivation, and partial attenuation of TGF-β1-associated fibrogenesis.

HMGB1 inhibition: The hepatoprotective effect of glycyrrhizin is mediated in part by inhibition of the HMGB1–TLR4 signaling axis. By blocking HMGB1, glycyrrhizin alleviates immunopathological liver injury.

Antiviral mechanisms: The antiviral mechanisms of glycyrrhizic acid include inhibition of viral replication and immunity regulation. It affects cellular signaling pathways such as protein kinase C and casein kinase II, and transcription factors such as activator protein 1 and NF-κB. From a pharmacological perspective, glycyrrhizin showed therapeutic potential for COVID-19 through binding to ACE2, down-regulating pro-inflammatory cytokines, inhibiting intracellular reactive oxygen species (ROS) accumulation, suppressing high respiratory tract output, and inducing endogenous interferons.

Endocrine/steroid-modulating actions: Glycyrrhizin metabolites inhibit type 2 11β-hydroxysteroid dehydrogenase (11βHSD2), which decomposes cortisol into inactive cortisone in the distal nephron, thereby inducing mineralocorticoid receptor activity. This mechanism underlies both certain therapeutic uses and significant adverse effects (see Safety section).

4. Pharmacokinetics and Bioavailability

Following oral administration, glycyrrhizin is hydrolyzed by intestinal microbiota to glycyrrhetinic acid (GA), a more lipophilic and membrane-permeable metabolite with enhanced biological activity. After oral administration of glycyrrhizin, the parent compound is not detectable in plasma at any time, but glycyrrhetic acid is detected at considerable concentrations, while glycyrrhetic acid is not detected in the plasma of germ-free animals. This confirms that intestinal bacterial hydrolysis is an essential step for oral absorption.

Among the several reported glycyrrhizin metabolites, 18β-glycyrrhetyl-3-O-sulfate is the major compound found in humans after licorice consumption, followed by glycyrrhetinic acid itself. These metabolites are highly bound to albumin in blood circulation and are predominantly excreted into bile via multidrug resistance-associated protein 2 (Mrp2).

In the case of tablets, it has been reported that glycyrrhizin is quickly decomposed into glycyrrhetinic acid in the stomach, and transfer of unchanged glycyrrhizin having high pharmacological activity into blood is hardly observed, making oral tablets far less effective compared to injection preparations. Glycyrrhizin belongs to a biological macromolecule with strong polarity, so the bioavailability of injection is higher than that of oral administration.

5. Scientific Evidence by Area of Use

5.1 Liver Disease and Hepatoprotection

The liver is the most extensively studied area of clinical application for glycyrrhizin. Glycyrrhizic acid has been used clinically for more than 20 years in patients with chronic hepatitis in China and Japan, and shows a satisfactory therapeutic effect in many other diseases.

Chronic Hepatitis C: In randomized controlled trials, glycyrrhizin induced a significant reduction of serum aminotransferases and an improvement in liver histology compared to placebo. In Japan, glycyrrhizin preparations (Stronger Neo-Minophagen C, SNMC) have been used for more than 20 years as a treatment for chronic hepatitis patients who do not respond to interferon therapy. However, in a double-blind, randomized, placebo-controlled trial involving 57 patients with hepatitis C, intravenous administration of 80–240 mg glycyrrhizin per day, three days per week for four weeks, improved serum alanine aminotransferase but had no effect on hepatitis C RNA levels.

Broader liver disease: Clinical studies have shown that glycyrrhizin injection therapy can successfully reduce the incidence of hepatocellular carcinoma and ALT levels in patients with chronic liver disease related to hepatitis C; when combined with conventional Western medicine in the treatment of acute icteric hepatitis, compound glycyrrhizin injection effectively improved patients' liver function parameters, markedly reducing total bilirubin, ALT, and AST levels, and was also more effective than conventional Western medicine alone in overall clinical symptom improvement and shortened the duration of jaundice by approximately 6 days.

Children with acute icteric hepatitis (meta-analysis): A meta-analysis found that compound glycyrrhizin injection plus conventional Western medicine might be better than conventional Western medicine alone in reducing ALT levels (MD = −24.09 U/L, 95% CI −30.83 to −17.34, P < 0.00001).

Limitations of evidence: A 2026 narrative review critically evaluated clinical evidence across major liver diseases and highlighted heterogeneity in study designs, geographical concentration of evidence (predominantly China and Japan), and the predominance of positive findings that may reflect publication bias. At present, the number of multicenter, large-sample, randomized, double-blind, controlled chemoprevention clinical trials with glycyrrhizic acid is very limited. Extensive clinical research is warranted to evaluate the safety and chemopreventive efficacy of glycyrrhizic acid alone or in combination with chemotherapy agents.

5.2 Antiviral Activity

In vitro antiviral effects have been observed for viruses causing respiratory tract infections, including influenza virus and the severe acute respiratory syndrome (SARS) coronavirus, as well as hepatitis B virus.

Hepatitis C virus (HCV) — in vitro: Glycyrrhizin has been used in Japan to treat patients with chronic viral hepatitis as an anti-inflammatory drug to reduce serum alanine aminotransferase levels. Glycyrrhizin is known to exhibit various biological activities including anti-viral effects. In one study, glycyrrhizin treatment of HCV-infected Huh7 cells caused a reduction of infectious HCV production. In cells treated with glycyrrhizin at non-toxic doses, the results demonstrated that glycyrrhizin inhibited HCV titer in a dose-dependent manner, resulting in a 50% reduction of HCV at a concentration of 14 ± 2 μg.

SARS-CoV-2 — preclinical and early clinical: The most frequent mechanism of the antiviral activity against SARS-CoV-2 is disrupting viral uptake into host cells and disrupting the interaction between the receptor-binding domain (RBD) of SARS-CoV-2 and ACE2. Fifty reviewed studies indicate that glycyrrhizin and licorice extract have significant antioxidant, anti-inflammatory, and immunomodulatory effects, and twenty-five studies provide evidence for the protective effect of glycyrrhizin and licorice extract against inflammation-induced acute lung injury and cardiovascular disorders. However, more randomized clinical trials are needed to obtain a precise conclusion.

While the potent antiviral and anti-inflammatory properties of glycyrrhizic acid and its derivatives in cellular and animal models are well-documented, their utilization for human respiratory tract infections remains limited.

5.3 Skin Conditions

Glycyrrhizin is widely used in skin disorders such as psoriasis, alopecia areata, and allergic diseases.

Chronic eczema — RCT: A multicenter, randomized, double-blind, placebo-controlled study in 199 patients with chronic eczema evaluated the efficacy of oral compound glycyrrhizin (OCG) plus topical corticosteroid (TCS), with participants from 6 centers in China receiving either 75 mg OCG capsules or placebo capsules three times a day and TCS (0.1% mometasone furoate ointment) once daily for 28 days. The combination therapy significantly improved the appearance of skin lesions, alleviated pruritus, and reduced disease recurrence, suggesting that OCG may be a nonsteroidal agent with an additional effect for the treatment of chronic eczema when used alongside topical corticosteroids.

Alopecia areata — RCT: One randomized controlled trial administered two oral tablets of 25 mg glycyrrhizin three times per day (tid) to the test group (65 patients) or two oral tablets of 25 mg cystine tid to the control (56 cases) for mild-to-moderate active alopecia areata. Compound glycyrrhizin has been noted for its diverse biological effects including anti-inflammatory and immunosuppressive properties, useful in therapy for a wide range of diseases such as chronic hepatitis, eczema, atopic dermatitis, and alopecia areata.

5.4 Anti-inflammatory and Immunomodulatory Effects

By acting on multiple targets in inflammatory pathways such as phospholipase A2 and high mobility group protein 1 (HMGB1), glycyrrhizin can inhibit the inflammatory response, reduce the pathological damage of the liver, and repair damaged liver cell function. Glycyrrhizin and its metabolite 18β-glycyrrhetinic acid are among the best-characterized constituents and have been linked to anti-inflammatory, antiviral, antioxidant, anti-apoptotic, and membrane-stabilizing activities. The majority of mechanistic data comes from in vitro cell culture and animal model studies; the direct translation of these mechanisms to specific human outcomes is less established outside of liver disease.

5.5 Antimicrobial Activity

Glycyrrhizin and its active metabolite glycyrrhetinic acid exhibit antibacterial, antiviral, and antibiofilm activity, acting through coordinated mechanisms including disrupting microbial membranes, inhibiting metabolic pathways, modulating efflux systems, suppressing biofilm structure, and regulating host inflammatory responses. Their ability to enhance antibiotic efficacy further supports their role as adjunctive therapeutic agents. This evidence remains predominantly preclinical (in vitro and animal models); robust human clinical trials in this area are lacking.

5.6 Metabolic Effects (Glucose Regulation)

Glycyrrhizic acid was reported to suppress the rise in fasting blood glucose and insulin levels and improve glucose tolerance. Additionally, glycyrrhizic acid may act as an antidiabetic substance without inducing side effects, although the mechanism remains unclear. This is based on preclinical evidence; robust human clinical trials specifically investigating glycyrrhizin for glucose regulation are not yet established.

5.7 Overall Evidence Strength

Some studies of licorice in people have been completed, but there is not enough high-quality evidence to clearly support its use for any specific health condition. The strongest clinical evidence relates to hepatoprotection and liver enzyme normalization in viral hepatitis, predominantly based on studies conducted in Asia. Evidence for antiviral, dermatological, and anti-inflammatory effects in humans is of lower quality, with most mechanistic data derived from in vitro and animal studies. A clear translational asymmetry exists: the antioxidant and inflammatory evidence base is relatively dense, but the fibrosis and clinical translation domains remain thinner.

6. Dosage Forms and Dosages Reported in Studies

Dosages and formulations vary substantially depending on route of administration and clinical indication:

• Intravenous (SNMC, hepatitis): In a double-blind, randomized, placebo-controlled trial, intravenous administration of 80–240 mg glycyrrhizin per day, three times per week for four weeks, was used in patients with hepatitis C.
• Oral (eczema): In the multicenter RCT for chronic eczema, participants received 75 mg OCG capsules three times daily (totalling 225 mg/day) alongside TCS for 28 days.
• Oral (alopecia areata): In the alopecia areata RCT, two oral tablets of 25 mg glycyrrhizin were given three times per day (150 mg/day total).
• Regulatory upper limits: The EU Scientific Committee for Food (SCF) declined to set an ADI for glycyrrhizin owing to inadequate toxicological information, but recommended that individuals limit their intake to 100 mg/day. The Japanese government recommends no more than 200 mg/day.
• Proposed acceptable daily intake: Based on in vivo and clinical evidence, one safety review proposed an acceptable daily intake of 0.015–0.229 mg glycyrrhizin/kg body weight/day.

7. Safety Considerations and Drug Interactions

7.1 Pseudoaldosteronism (Primary Safety Concern)

Hypokalemia or pseudoaldosteronism (PsA) is one of the most frequent side effects of licorice intake. Glycyrrhizin metabolites inhibit type 2 11β-hydroxysteroid dehydrogenase (11βHSD2), which decomposes cortisol into inactive cortisone in the distal nephron, thereby inducing mineralocorticoid receptor activity.

The clinical presentation of pseudoaldosteronism is similar to that of primary aldosteronism and is characterized by peripheral edema, hypertension, laboratory hypokalemia, and lower plasma renin activity. The mineralocorticoid receptor stabilizes epithelial sodium channels, which increases sodium reabsorption, corresponding to peripheral edema, hypertension, and lower plasma renin activity, whereas potassium is excreted, resulting in hypokalemia and, in severe cases, myopathy or arrhythmia.

Pseudohyperaldosteronism due to licorice toxicity can mimic the features of primary aldosteronism without elevation of serum aldosterone concentration: electrolyte abnormalities may include hypokalemia, hypernatraemia, metabolic alkalosis, and acute kidney injury; neuromuscular manifestations can include paralysis, epileptiform manifestations, altered level of consciousness, rhabdomyolysis, and elevated CK level; cardiovascular effects can include ECG changes such as QT interval prolongation, U waves, slight ST segment elevation, supraventricular tachycardia, as well as hypertension, heart failure, pulmonary oedema, and cardiac death (two cases).

Most cases of licorice-induced pseudoaldosteronism are self-limiting and are resolved once licorice intake ceases, without any specific treatment. However, some cases can progress to severe hypokalemia and life-threatening arrhythmia.

7.2 Dose-Dependency and Susceptibility Factors

High dosage and long-term use of licorice are constitutional risk factors for pseudoaldosteronism. Several studies have reported that excessive or long-term consumption of glycyrrhizin can induce adverse effects such as hypertension, hypokalemia, and sodium retention. Pharmacokinetic modeling indicates that the risk of adverse effects increases abruptly above 101 mg, making this the critical dose limit of glycyrrhizin causing hypokalemia in the elderly with a probability of 3.07%.

The widespread presence of glycyrrhizin in food, beverages, and herbal products represents a growing toxicological concern. The inhibitory effect on 11β-HSD2 occurs even at low glycyrrhetinic acid concentrations; the direct effect on mineralocorticoid receptors is usually negligible and therefore is only observed in cases of chronic overconsumption.

Hepatic dysfunction, alcohol use disorder, and interindividual metabolic variability can markedly delay glycyrrhetinic acid elimination, increasing the risk of persistent toxicity even with moderate exposure.

Orally administered glycyrrhizin is more effectively hydrolyzed to glycyrrhetinic acid by the intestinal bacteria in constipated patients, which enhances the bioavailability of glycyrrhizin metabolites and thus may amplify adverse effects at a given dose.

7.3 Cardiovascular and Hypertensive Effects

Biochemical studies indicate that glycyrrhizinates inhibit 11β-hydroxysteroid dehydrogenase, the enzyme responsible for inactivating cortisol. As a result, continuous, high-level exposure to glycyrrhizin compounds can produce hypermineralocorticoid-like effects in both animals and humans. Licorice- and glycyrrhizin-induced hypertension due to pseudo-hyperaldosteronism has been widely reported. Glycyrrhizin can induce hypertensive crisis with target organ impairment, reminding clinicians of a condition which could lead to medical emergencies.

7.4 Drug Interactions

Biochemical studies indicate that glycyrrhizinates inhibit 11β-hydroxysteroid dehydrogenase, the enzyme responsible for inactivating cortisol. This mechanism creates a potential for interaction with corticosteroid medications, as glycyrrhizin can prolong and amplify the action of endogenous and exogenous corticosteroids. Glycyrrhetinic acid has been reported to alter several other enzymatic processes, including inhibition of mitochondrial oxidative phosphorylation, cytochrome P450 monooxygenase systems, and N-acetyltransferase activity, suggesting a theoretical basis for interactions with drugs that are substrates of these pathways.

The continuous, high-level exposure to glycyrrhizin compounds can produce hypermineralocorticoid-like effects, and these effects are reversible upon withdrawal. Due to its blood pressure-raising and potassium-depleting properties, glycyrrhizin has a documented potential to antagonize antihypertensive drugs and exacerbate effects of diuretics or other potassium-depleting agents.

7.5 Regulatory Status and GRAS Designation

Glycyrrhizinic acid is currently considered "Generally Recognized as Safe" (GRAS) by the US Food and Drug Administration, and there is a guideline for maximum permitted levels of the saponin in several preparations. There is a high level of use of licorice and glycyrrhizin in the US with an estimated consumption of 0.027–3.6 mg glycyrrhizin/kg/day. Both licorice and glycyrrhizin products have been approved for use in foods by most national and supranational regulatory agencies.

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